Previous studies have shown that a red seaweed extract, carrageenan, produces colonic ulcerations in guinea pigs which simulates ulcerative colitis in humans. Sequential bacteriologic analysis of animals receiving a 5% oral solution of carrageenan revealed major increases in both the obligately anaerobic and coliform populations in the colon. Antimicrobial probes directed against various components of the flora were used to selectively suppress selected bacterial populations in order to define their role in the experimental model. Both clindamycin and metronidazole, which are active against anaerobes, were effective in preventing cecal ulceration. Gentamicin and co-trimoxazole, while suppressing the coliform population, were ineffective in preventing ulceration. Delayed use of metronidazole was ineffective in decreasing the severity of already formed cecal ulcerations. These data suggest that obligate anaerobes play a role in initiation of the events culminating in ulceration, but elimination of this microflora once ulceration is present does not serve a therapeutic function in this animal model. Additonal studies using caesarian derived gnotobiotic guinea pigs suggest that carrageenan alone is not responsible for ulceration since these animals do not develop cecal ulceration. Studies in which selected bacterial species are added to the gnotobiotic gut microflora are in progress in an effort to identify the species which contribute to cecal ulceration. BIBLIOGRAPHIC REFERNCE: Onderdonk, A.B., Hermos, J.A., Dzink, J.L., Bartlett, J.G., Antimicrobial Probes in Experimental Ulcerative Colitis: Protection with Metronidazole. 1977. Clin. Res., (in press).